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Experiments were conducted to compare a short-term 48-h aquatic toxicity test endpoint of abnormal larval shell development with other, more clearly adverse effects. In similar experiments conducted with two different toxicants, zinc sulfate and bleached-kraft mill effluent, red abalone (Haliotis rufescens) embryos were simultaneously exposed to identical dilution series and incubated for three different exposure periods: 48 h, 48 h followed by an 8-d recovery period in clean seawater, and 10 d of continuous exposure. Abnormal larval shell development was assessed in the 48-h short-term tests, and inhibition of metamorphosis was assessed in the exposure-recovery and continuous exposure experiments. For the zinc experiments, the median effective concentration (EC50) values for the 48-h exposure the exposure-recovery experiment, and the continuous exposure experiment were 40, 34, and 32 μg/L zinc, respectively. For the bleached- kraft mill effluent experiments, the EC50 values were 0.98, 0.76, and 0.69% effluent, respectively. Results indicate that toxicant concentrations causing abnormal larval shell development also inhibit metamorphosis and that larvae exposed to toxicant concentrations which inhibit larval shell development do not recover to metamorphose when transferred to clean seawater. None of the successfully metamorphosed postlarvae had deformed larval shells, indicating that shell deformity precludes survival past the planktonic stage. A longer (15-d) experiment allowed measurement of postlarval shell length in exposed postmetamorphic abalone. Insignificant differences in postlarval shell length indicated that the timing of larval metamorphosis was similar regardless of toxicant exposure and that the effects of the toxicant was to inhibit rather than to delay metamorphosis., Cited By (since 1996):27, CODEN: ETOCD, ,